An inertial range length scale in structure functions

It is shown using experimental and numerical data that within the traditional inertial subrange defined by where the third order structure function is linear that the higher order structure function scaling exponents for longitudinal and transverse structure functions converge only over larger scales, $r>r_S$, where $r_S$ has scaling intermediate between $\eta$ and $\lambda$ as a function of $R_\lambda$. Below these scales, scaling exponents cannot be determined for any of the structure functions without resorting to procedures such as extended self-similarity (ESS). With ESS, different longitudinal and transverse higher order exponents are obtained that are consistent with earlier results. The relationship of these statistics to derivative and pressure statistics, to turbulent structures and to length scales is discussed.Comment: 25 pages, 9 figure

Local properties of extended self-similarity in 3D turbulence

Using a generalization of extended self-similarity we have studied local scaling properties of 3D turbulence in a direct numerical simulation. We have found that these properties are consistent with lognormal-like behavior of energy dissipation fluctuations with moderate amplitudes for space scales $r$ beginning from Kolmogorov length $\eta$ up to the largest scales, and in the whole range of the Reynolds numbers: $50 \leq R_{\lambda} \leq 459$. The locally determined intermittency exponent $\mu(r)$ varies with $r$; it has a maximum at scale $r=14 \eta$, independent of $R_{\lambda}$.Comment: 4 pages, 5 figure

Strong Universality in Forced and Decaying Turbulence

The weak version of universality in turbulence refers to the independence of the scaling exponents of the $n$th order strcuture functions from the statistics of the forcing. The strong version includes universality of the coefficients of the structure functions in the isotropic sector, once normalized by the mean energy flux. We demonstrate that shell models of turbulence exhibit strong universality for both forced and decaying turbulence. The exponents {\em and} the normalized coefficients are time independent in decaying turbulence, forcing independent in forced turbulence, and equal for decaying and forced turbulence. We conjecture that this is also the case for Navier-Stokes turbulence.Comment: RevTex 4, 10 pages, 5 Figures (included), 1 Table; PRE, submitte

Anomalous scaling, nonlocality and anisotropy in a model of the passively advected vector field

A model of the passive vector quantity advected by a Gaussian time-decorrelated self-similar velocity field is studied; the effects of pressure and large-scale anisotropy are discussed. The inertial-range behavior of the pair correlation function is described by an infinite family of scaling exponents, which satisfy exact transcendental equations derived explicitly in d dimensions. The exponents are organized in a hierarchical order according to their degree of anisotropy, with the spectrum unbounded from above and the leading exponent coming from the isotropic sector. For the higher-order structure functions, the anomalous scaling behavior is a consequence of the existence in the corresponding operator product expansions of ``dangerous'' composite operators, whose negative critical dimensions determine the exponents. A close formal resemblance of the model with the stirred NS equation reveals itself in the mixing of operators. Using the RG, the anomalous exponents are calculated in the one-loop approximation for the even structure functions up to the twelfth order.Comment: 37 pages, 4 figures, REVTe

LY294002 may overcome 5-FU resistance via down-regulation of activated p-AKT in Epstein-Barr virus-positive gastric cancer cells

<p>Abstract</p> <p>Background</p> <p>As EBV-associated gastric cancer has unique features that are different from EBV (-) gastric cancer, EBV is considered to have a key role in gastric carcinogenesis. It has been reported that viral latent membrane protein 2A (LMP2A) in EBV-transformed tumor cells activates the phosphatidylinositol 3-kinase (PI3K)/AKT pathway, which provides a survival signal and chemo-resistance to cytotoxic anti-cancer drugs. This study was to evaluate anti-proliferative effect and cell cycle change when 5-FU and LY294002 (LY), a selective inhibitor of PI3K, were treated separately or combined with different schedules in EBV positive gastric cancer cell line, SNU-719.</p> <p>Methods</p> <p>After single treatment and sequential combination of 5-FU and LY, cytotoxic activity was measured by MTS assay. When 5-FU and LY were treated in single and sequential combinations, the expression of p-AKT, p-NFkB, p-p53 and bcl-2 was observed on different concentrations by Western blot analysis. We also investigated the effect on apoptosis and cell cycle distribution using flow cytometry. The LMP2A siRNA inhibition was done to confirm the reversal of decreased 5-FU activity and p-AKT.</p> <p>Results</p> <p>When 5-FU was sequentially combined with LY, the combination index (CI) value indicated synergistic anti-proliferative effect. The expression of p-AKT and p-NFκB was upregulated by 5-FU alone but sequential treatment of 5-FU and LY decreased the expression of both p-AKT and p-NFκB. When 5-FU was combined with LY, G0/G1 and sub G1 cell population (%) increased. When 5-FU was added to the cells transfected with LMP2A siRNA, its anti-proliferative effect increased and the expression of p-AKT decreased. In sequential combination of 5-FU and LY, the expression of p-p53 was increased and bcl-2 expression was diminished compared to 5-FU alone.</p> <p>Conclusion</p> <p>These data suggest that sequential combination of 5-FU and LY induce synergistic cytotoxicity and overcome intrinsic and acquired resistance of 5-FU via downregulation of activated p-AKT and mitochondria-dependent apoptosis in EBV gastric cancer cell line, SNU-719.</p

Delayed Re-Epithelialization in Periostin-Deficient Mice during Cutaneous Wound Healing

BACKGROUND: Matricellular proteins, including periostin, are important for tissue regeneration. METHODS AND FINDINGS: Presently we investigated the function of periostin in cutaneous wound healing by using periostin-deficient ⁻/⁻ mice. Periostin mRNA was expressed in both the epidermis and hair follicles, and periostin protein was located at the basement membrane in the hair follicles together with fibronectin and laminin γ2. Periostin was associated with laminin γ2, and this association enhanced the proteolytic cleavage of the laminin γ2 long form to produce its short form. To address the role of periostin in wound healing, we employed a wound healing model using WT and periostin⁻/⁻ mice and the scratch wound assay in vitro. We found that the wound closure was delayed in the periostin⁻/⁻ mice coupled with a delay in re-epithelialization and with reduced proliferation of keratinocytes. Furthermore, keratinocyte proliferation was enhanced in periostin-overexpressing HaCaT cells along with up-regulation of phosphorylated NF-κB. CONCLUSION: These results indicate that periostin was essential for keratinocyte proliferation for re-epithelialization during cutaneous wound healing